A murine model of variant late infantile ceroid lipofuscinosis recapitulates behavioral and pathological phenotypes of human disease

Keyphrases

• Murine Model 100%
• Human Disease 100%
• Neuronal Ceroid Lipofuscinosis 100%
• Behavioral Phenotype 100%
• CLN6 100%
• Late Infantile 100%
• Pathological Phenotype 100%
• Cortex 66%
• Hippocampus 33%
• Mouse Model 33%
• Endoplasmic Reticulum 33%
• Autosomal Recessive 33%
• Seizure 33%
• Early Onset 33%
• Membrane Protein 33%
• Lysosomal Storage Disease 33%
• Motor Dysfunction 33%
• Cerebral Cortex 33%
• Adult-onset 33%
• Cognitive Dysfunction 33%
• Motor Learning 33%
• Neuron Loss 33%
• Lamin 33%
• Translational Research 33%
• Potential Therapeutics 33%
• Motor Coordination 33%
• Premature Death 33%
• Motor Memory 33%
• GABAergic Interneurons 33%
• Glial Activation 33%
• Batten Disease 33%
• Dendritic Spine Density 33%
• Non-glycosylated 33%
• Unknown Protein 33%
• Visual Impairment 33%
• Visual-motor 33%
• Infantile Onset 33%
• Clinical Symptomatology 33%
• Visual Cognition 33%
• Screened Potential 33%
• Glycosylated Membrane 33%
• Interneuron Subpopulations 33%
• Synaptic Strength 33%

Neuroscience

• Neuronal Ceroid Lipofuscinosis 100%
• Ceroid 100%
• Hippocampus 50%
• Cognitive Disorders 50%
• Stereotypic Movement Disorder 50%
• Cerebral Cortex 50%
• Motor Learning 50%
• Motor Coordination 50%
• Dendritic Spine 50%
• Interneuron 50%
• Endoplasmic Reticulum 50%
• Synaptic Strength 50%

Biochemistry, Genetics and Molecular Biology

• Batten Disease 100%
• Neuronal Ceroid Lipofuscinosis 66%
• Mouse Model 33%
• Membrane Protein 33%
• Autosomal Recessive Inheritance 33%
• Interneuron 33%
• Motor Coordination 33%
• Motor Learning 33%
• Dendritic Spine 33%